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Coronary plaques calling for action — why, where and how many?

J.F. Bentzon and E. Falk*

Department of Cardiology, Research Unit, Aarhus University Hospital (Skejby), DK-8200 Aarhus N, Denmark

* Correspondence: Professor Erling Falk, MD, PhD, Department of Cardiology, Research Unit, Aarhus University Hospital (Skejby), DK-8200 Aarhus N, Denmark.

Abstract

Aims Most adults of the Western World harbour advanced atherosclerotic plaques in their coronary arteries, and many will eventually suffer an acute coronary syndrome. The majority, however, will not. This overview sets out to answer the question: Why do some plaques rupture and become the culprit of an acute coronary syndrome whereas most do not?

Methods and Results At least part of the answer has been elucidated through meticulous autopsy studies. The risk of plaque rupture appears to depend on plaque morphology rather than plaque size or severity of stenosis. Fibrosis with smooth muscle cell proliferation and collagen synthesis hardens the plaque, stabilizing it against rupture, while inflammation leading to degradation of the fibrous cap and growth of the soft core predisposes the plaque to rupture.

Conclusions Traditionally, plaque vulnerability has been viewed as a focal disorder calling for a target-lesion based approach. However, accumulating data indicate that multiple ruptured plaques are the rule rather than the exception in patients who die from atherosclerosis, and that multiple luminal thrombi are not rare. If plaque vulnerability changes for the entire arterial tree as a whole, rather than focally, this calls for systemic treatment modalities.

Key Words: Atherosclerosis • fibrosis • inflammation • local factors • plaque rupture • systemic factors

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